神经生长因子（NGF）介导的神经元存活是否需要钠钾泵的激活？
Is activation of the Na+K+ pump necessary for NGF-mediated neuronal survival?
作者信息
Sendtner M, Gnahn H, Wakade A, Thoenen H
机构信息
Max-Planck-Institute for Psychiatry, Department of Neurochemistry, Martinsried, Federal Republic of Germany.
出版信息
J Neurosci. 1988 Feb;8(2):458-62. doi: 10.1523/JNEUROSCI.08-02-00458.1988.
The ability of nerve growth factor to cause rapid activation of the Na+K+ pump of its responsive cells was examined by measuring the uptake of 86Rb+. A significant increase in 86Rb+ uptake in E8 chick dorsal root ganglion sensory neurons after NGF treatment was seen only if the cells had been damaged during the preparation procedure. Such damaged cells could not survive in culture in the presence of NGF, and undamaged cells that did survive in response to NGF exhibited no increased 86Rb+ uptake rate. Furthermore, cultured calf adrenal medullary cells did not show an increase in 86Rb+ uptake after treatment with NGF, although these cells respond to NGF with an increased synthesis of catecholaminergic enzymes. These results are incompatible with the hypothesis that the mechanism of action of NGF that promotes neuronal survival and enzyme induction results from an initial stimulation of the Na+K+ pump.
通过测量⁸⁶Rb⁺的摄取量，研究了神经生长因子引起其反应性细胞的Na⁺K⁺泵快速激活的能力。仅当细胞在制备过程中受到损伤时，才会观察到在神经生长因子处理后，E8期鸡背根神经节感觉神经元中⁸⁶Rb⁺摄取量显著增加。此类受损细胞在神经生长因子存在的情况下无法在培养中存活，而对神经生长因子有反应并存活下来的未受损细胞，其⁸⁶Rb⁺摄取率并未增加。此外，培养的小牛肾上腺髓质细胞在用神经生长因子处理后，⁸⁶Rb⁺摄取量并未增加，尽管这些细胞对神经生长因子的反应是儿茶酚胺能酶的合成增加。这些结果与以下假设不一致，即神经生长因子促进神经元存活和酶诱导的作用机制源于对Na⁺K⁺泵的初始刺激。
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